Claritin-D Interactions
Alpha-blockers
- Ammonium Chloride
Anti-retroviral protease inhibitors
Antidiabetic Agents
Beta-blockers
- Bromocriptine
- Caffeine
Cardiac glycosides
Central-acting adrenergic agents
- Cimetidine
- Citric Acid; Sodium Citrate
- Clarithromycin
- Cocaine
- Cyclopropane
- Delavirdine
- Dronabinol, THC
- Efavirenz
Ergot Alkaloids
- Erythromycin
- Fluconazole
- Furazolidone
- Green Tea
- Guarana
Halogenated anesthetics
- Imatinib, STI-571
- Itraconazole
- Ketoconazole
- Linezolid
- Mecamylamine
- Methazolamide
- Miconazole
Monoamine oxidase inhibitors (MAOIs)
- Nefazodone
Nitrates
- Potassium Citrate
- Procarbazine
- Reserpine
- Sodium Acetate
- Sodium Bicarbonate
- Sodium Lactate
- St. John’s Wort, Hypericum perforatum
Sympathomimetics
- Theophylline, Aminophylline
Thyroid hormones
Tricyclic antidepressants
- Voriconazole
Claritin-D Interactions
Due to its pseudoephedrine component, this product should not be used by patients receiving monoamine oxidase inhibitors or within 14 days of stopping use of an MAO inhibitor. MAOIs, or drugs that possess MAO-inhibiting activity such as furazolidone, linezolid, or procarbazine, can prolong and intensify the cardiac stimulation and vasopressor effects of pseudoephedrine. Phenelzine and tranylcypromine appear to produce the greatest risk since these 2 MAOIs also have intrinsic amphetamine-like activity. In the presence of MAOIs, pseudoephedrine and other drugs that cause release of norepinephrine induce severe cardiovascular and cerebrovascular responses. It is unclear if selegiline, an inhibitor of MAO type B, can also predispose to this reaction.
Cimetidine, erythromycin, nefazodone and ketoconazole have been shown to interfere with the metabolism of loratadine, probably through inhibition of the cytochrome P-450 (CYP) 3A4 isozyme, resulting in increased serum concentrations of loratadine and its metabolite. Theoretically, other systemic azole antifungals (e.g., fluconazole, itraconazole, IV miconazole, or voriconazole) could also lead to elevated levels of loratadine due to CYP3A4 inhibition. Elevated loratadine serum concentrations do not result in clinically significant QT prolongation, ECG changes, or any significant differences in adverse reactions compared to control patients. However, caution should be exercised with using this drug combination in a patient with concurrent risk factors for arrhythmogenic events. Although significant drug interactions have not been confirmed between loratadine and other agents that inhibit cytochrome P-450, caution should be used when loratadine is administered with highly potent CYP3A4 inhibitors due to the serious nature of interactions between these drugs and certain other H1-antagonists. Examples of potent CYP3A4 inhibitors not previously mentioned include: anti-retroviral protease inhibitors, clarithromycin, delavirdine, efavirenz (inhibits or induces), or imatinib, STI-571. This list is not inclusive of all potent CYP3A4 inhibitors.
Pseudoephedrine can potentiate the effects and increase the toxicity of other sympathomimetics including cocaine by adding to their sympathomimetic activity. Although no data are available, pseudoephedrine should be used cautiously in patients using significant quantities of amphetamines, cocaine, or other sympathomimetics. Concurrent use of dronabinol, THC with sympathomimetics may result in additive hypertension, tachycardia, and possibly cardiotoxicity.
The cardiovascular effects of sympathomimetics may reduce the antihypertensive effects of produced by reserpine, alpha-blockers, beta-blockers, central-acting adrenergic agents (e.g., clonidine, guanfacine, guanabenz, methyldopa), and mecamylamine. Blood pressure should be monitored closely to confirm that the desired antihypertensive effect is achieved. Increased ectopic pacemaker activity can occur when pseudoephedrine is used concomitantly with cardiac glycosides. Pseudoephedrine may also interact with many tricyclic antidepressants resulting in increased risk for severe headaches or cardiovascular toxicity.
Although loratadine is considered a ‘non-sedating’ antihistamine, dose-related sedation has been noted. For this reason, it would be prudent to monitor for drowsiness when loratadine; pseudoephedrine is used concurrently with other CNS depressants such as barbiturates, benzodiazepines, opiate agonists, antipsychotics, tricyclic antidepressants, ethanol, other sedating H1-blockers, and anxiolytics, sedatives, and hypnotics.
Concomitant use of nitrates with sympathomimetics can result in antagonism of the antianginal effects of the nitrate.
Concurrent administration of caffeine with pseudoephedrine can produce excessive stimulatory effects such as nervousness, irritability, insomnia, or tremor. Other xanthines, such as theophylline, can interact in a similar way. Excessive caffeine ingestion should be avoided while taking pseudoephedrine concurrently. This includes ingestion of foods and beverages that contain high amounts of caffeine such as coffee, teas, green tea, colas, and chocolate and dietary supplements such as guarana.
Where possible, avoid concurrent use of pseudoephedrine-containing products and the ergot alkaloids. Although no data are available, it is possible that concomitant use of pseudoephedrine with ergotamine or dihydroergotamine could cause additive and possibly severe peripheral vasoconstriction. Some ergot alkaloids, notably ergotamine and, to a lesser extent, ergonovine, may produce peripheral vasoconstriction due to alpha-receptor agonism in the peripheral circulation. Hypertension, headache, myocardial ectopy, and seizures have occurred when bromocriptine, an ergot derivative, was combined with various sympathomimetics. Pseudoephedrine use should be avoided in patients on ergot alkaloids or bromocriptine whenever possible.
Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Ammonium chloride, by acidifying the urine, increases the elimination of pseudoephedrine while sodium bicarbonate, a urinary alkalinizer, allows for increased tubular reabsorption of pseudoephedrine. While the interaction with ammonium chloride is unlikely to be clinically signficant, concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions. Other urinary alkalinizers include sodium citrate, potassium citrate, sodium lactate, and sodium acetate.
Methazolamide can decrease excretion and enhance the effects of pseudoephedrine. Carbonic anhydrase inhibitors increase the alkalinity of the urine, thereby increasing the amount of nonionized pseudoephedrine available for renal tubular reabsorption. Use caution if methazolamide is coadministered; monitor for excessive pseudoephedrine-related adverse effects.
Pseudoephedrine may increase blood sugar via stimulation of beta2-receptors which leads to increased glycogenolysis. A pharmacodynamic interaction with antidiabetic agents may occur. Patients receiving antidiabetic agents should be closely monitored for loss of diabetic control when therapy with sympathomimetic agents is instituted.
Drug interactions with St. John’s wort, Hypericum perforatum are unclear at this time. Some of the components of this herb have been shown to inhibit monoamine oxidase (MAO) in vitro, but in vivo activity is unclear. If St. John’s wort does have MAOI-like activities, it could potentially increase the cardiac stimulation and vasopressor effects of the sympathomimetics. St. John’s wort should be used cautiously with any sympathomimetic agent.
Concomitant use of sympathomimetics and thyroid hormones can enhance the effects of either drug on the cardiovascular system. Patients with coronary artery disease have an increased risk of coronary insufficiency from either agent. Combined use of these agents may further increase this risk.
Halogenated anesthetics and cyclopropane may sensitize the myocardium to the effects of sympathomimetics, including pseudoephedrine.
[ Last revised: 9/27/2004 5:32:00 PM ]
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